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Department of Microbiology, Boston University School of Medicine, Boston, MA 02118
The effect of vitamin E on mitogenesis by polyclonal activators was studied and the vitamin was found to be stimulatory but selective in its action. Vitamin E itself is a mitogen for murine spleen cells. At suboptimal vitamin concentrations, it was capable of stimulating the response to low levels of the thymus-dependent lymphocyte (T cell) mitogen, concanavalin A (conA), but not when conA was itself at optimal levels. When vitamin E was added to the diet at normal levels, it was not as effective in stimulating mitogenesis as it was at much higher levels. The effect of the vitamin on T cell mitogenesis could be modified by the degree of unsaturation of the dietary fat; it was more effective when dietary polyunsaturated fatty acids (PUFA) were low. Under several conditions, it was shown that vitamin E can increase the phytohemagglutinin (PHA)/conA response ratio, which may suggest an effect of the vitamin on the maturation of T cells. In normal mice, vitamin E also stimulated the response to lipopolysaccharide (LPS), a "bursa-equivalent" lymphocyte (B cell) mitogen, but it was unable to do so when spleen cells from athymic, nude mice were used. This suggests a requirement for thymic factors in order for vitamin E to stimulate mitogenesis of B cells.
KEY WORDS: vitamin E mitogenesis polyunsaturated fatty acids (PUFA) lymphocytes T cells B cells
1 Supported by a grant from NIH, AM21618, and a grant from Hoffmann La Roche Inc.
Manuscript received 27 August 1979.